Treatment of cells with DNA damaging agents leads to large-scale gene expression changes. Proper transcriptional regulation is important for cells to arrest, repair damage and adjust cellular processes such as metabolism in order to survive the damaging assault. Damage-induced transcription is a highly regulated response. This study establishes a novel role for two factors, Snf1 and Rad23, in regulation of the UV-induced transcriptional response.
No associated publication
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View SamplesTumors of advanced gastric cancer patients were biopsied and subjected to gene expression profiling using the Affymetrix Human Genome U133 Plus 2.0 Arrays. Patients were then segregated into G1, G2 or G3 groups based on their tumor genomic profiles. Patients in the G1 and G3 cohorts were assigned SOX (oxaliplatin plus S-1) chemotherapy whereas those in the G2 cohort were given SP (cisplatin plus S-1) regimen.
Real-Time Tumor Gene Expression Profiling to Direct Gastric Cancer Chemotherapy: Proof-of-Concept "3G" Trial.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Proteomic analysis of Medulloblastoma reveals functional biology with translational potential.
Sex, Specimen part
View SamplesThese gene expression microarrays were performed as part of a project aiming to integrate quantitative proteomic, gene expression and epigenetic data from the childhood brain tumor medulloblastoma.
Proteomic analysis of Medulloblastoma reveals functional biology with translational potential.
Sex, Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Gene reactivation by 5-aza-2'-deoxycytidine-induced demethylation requires SRCAP-mediated H2A.Z insertion to establish nucleosome depleted regions.
Specimen part, Disease, Disease stage, Cell line, Treatment
View SamplesRepair of injured muscle involves repair of injured myofibers through the involvement of dysferlin and its interacting partners, including annexin. Studies with mice and patients have established that dysferlin deficit leads to chronic inflammation and adipogenic replacement of the diseased muscle. However, longitudinal analysis of annexin deficit on muscle pathology and function is lacking. Here we show that unlike annexin A1, but similar to dysferlin, lack of annexin A2 (AnxA2) causes poor myofiber repair and progressive weakening with age. However, unlike dysferlin-deficient muscle, AnxA2-deficient muscles do not exhibit chronic inflammation or adipogenic replacement. Deletion of AnxA2 in dysferlin deficient mice reduces inflammation, adipogenic replacement, and loss in muscle function caused by dysferlin deficit. These results show that: a) AnxA2 facilitates myofiber repair, b) chronic inflammation and adipogenic replacement of dysferlinopathic muscle requires AnxA2, and c) inhibiting AnxA2-mediated inflammation is a novel therapeutic avenue for dysferlinopathy.
Annexin A2 links poor myofiber repair with inflammation and adipogenic replacement of the injured muscle.
Age, Specimen part
View SamplesGenome wide gene expression profiling of RKO cells with combination treatments of non-target siRNA or SRCAP siRNA and PBS or 1uM 5-Aza-CdR treatment. The sample treated with non target siRNA and PBS serves as control sample.
No associated publication
Specimen part, Disease, Disease stage, Cell line
View SamplesCells were treated with MK591 and gene expression was analyzed with Illumina bead chip array.
No associated publication
Specimen part, Cell line
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Epstein-Barr virus-associated primary nodal T/NK-cell lymphoma shows a distinct molecular signature and copy number changes.
Disease, Disease stage
View SamplesTo investigate if biologically distinct subsets exists in extranodal NK/T-cell lymphoma (NKTL), we performed unsupervised integrative analyses of gene expression profiling (GEP), miRNA profiling, and copy number aberration (CNA) on 66 cases of NKTL from diverse anatomical sites. This series is the GEP data.
Epstein-Barr virus-associated primary nodal T/NK-cell lymphoma shows a distinct molecular signature and copy number changes.
Disease, Disease stage
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